title: Involvement of endothelin-1 in habitual exercise-induced increase in arterial compliance.
abstract: OBJECTIVE
  Habitual aerobic exercise results in a significant increase in central arterial compliance. Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor peptide and could play a role in mediating the habitual aerobic exercise-induced increase in central arterial compliance. The aim of the present study was to examine whether ET-1 is involved in the mechanisms underlying the increase in central arterial compliance with aerobic exercise training.
  
  
  METHODS
  Seven apparently healthy middle-aged and older (60 +/- 3 years) adults underwent systemic endothelin-A/B (ET(A/B))-receptor blockade (500 mg of Tracleer) before and after 12 weeks of aerobic exercise training (70 +/- 1% of maximal heart rate, 44 +/- 2 min day(-1), 4.4 +/- 0.1 days week(-1)).
  
  
  RESULTS
  Basal carotid arterial compliance (via simultaneous B-mode ultrasound and arterial applanation tonometry on the common carotid artery) increased significantly after exercise training. Resting plasma ET-1 concentration decreased significantly after exercise training. Before exercise intervention, carotid arterial compliance increased significantly with the administration of the ET(A/B)-receptor blockade. After training, however, increases in carotid arterial compliance previously observed with the ET(A/B)-receptor blockade before training were abolished.
  
  
  CONCLUSIONS
  Regular aerobic exercise training enhances central arterial compliance in middle-aged and older humans. The increase in arterial compliance was associated with the corresponding reduction in plasma ET-1 concentration as well as the elimination of ET-1-mediated vascular tone. These results suggest that reductions in ET-1 may be an important mechanism underlying the beneficial effect of exercise training on central artery compliance.
authors.affiliation: Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Ibaraki, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Maeda
authors.forename: J
authors.initials: J
authors.lastname: Sugawara
authors.forename: M
authors.initials: M
authors.lastname: Yoshizawa
authors.forename: T
authors.initials: T
authors.lastname: Otsuki
authors.forename: N
authors.initials: N
authors.lastname: Shimojo
authors.forename: S
authors.initials: S
authors.lastname: Jesmin
authors.forename: R
authors.initials: R
authors.lastname: Ajisaka
authors.forename: T
authors.initials: T
authors.lastname: Miyauchi
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000273:Adipose Tissue / Q000502:physiology; D000368:Aged; D000959:Antihypertensive Agents / Q000494:pharmacology; D001158:Arteries / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D001786:Blood Glucose / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D000077300:Bosentan; D002339:Carotid Arteries / Q000033:anatomy & histology; D002784:Cholesterol / Q000097:blood; D003187:Compliance / Q000187:drug effects / Q000502:physiology; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1 / Q000037:antagonists & inhibitors / Q000097:blood*; D015444:Exercise / Q000502:physiology*; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: D000959:Antihypertensive Agents; D001786:Blood Glucose; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1; D013449:Sulfonamides; D002784:Cholesterol; D000077300:Bosentan